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77 publications mentioning mmu-mir-199b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-199b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 466
Overall, we assessed the levels of persistence of adenovirus expression in infected cells, as the down-regulation of HES1 expression due to miR199b carrying the adenovirus expression, thus following tumor growth over time by BLI see Figure 4G–H, and antibodies staining Figure S4L–M (Hes1, Ki67, Gabra6, Nestin, Math-3, see details in Text S1 information). [score:10]
It will be of interest for future studies to also determine the down-regulation of this target by miR-199b, even if it appears unlikely because of the lack of induction of apoptosis after miR-199b over -expression in our cellular systems. [score:8]
When miR-199b-5p over -expression in Daoy cells was examined for down-regulation of productive translation from a reporter gene carrying the full-length 3′UTRs indicated, none of them were seen to be affected. [score:8]
Down-regulation of HES1 expression by miR-199b-5p negatively regulates the proliferation rate and anchorage-independent growth of MB cells. [score:7]
The analysis of miR-199b-5p expression in two MB cell lines, human adult tissue and mouse cerebellum, is shown in Text S1, Fig. S1C, D and S2A, B. To determine whether HES1 is a target of miR-199b-5p, the HES1 3′UTR was cloned downstream of a luciferase reporter gene vector; pre-miR-199b-5p was also cloned in a mammalian expression vector (see Text S1). [score:7]
D) Representative MiR-199b-5p expression profiles across a panel of human tissues (Ambion); miR-199b-5p was expressed to different degrees, with relatively high expression in the duodenum, lymph nodes, lung, skeletal muscle, right ventricle (highest), kidney, total heart and thyroid. [score:7]
The analysis of miR-199b-5p expression in two MB cell lines, human adult tissue and mouse cerebellum, is shown in Text S1, Fig. S1C, D and S2A, B. To determine whether HES1 is a target of miR-199b-5p, the HES1 3′UTR was cloned downstream of a luciferase reporter gene vector; pre-miR-199b-5p was also cloned in a mammalian expression vector (see Text S1). [score:7]
The levels of expression of mature miR-199b-5p are given relative to let-7A, with the data shown as means±SD from two independent experiments, each carried out in triplicates C) Representative Western blot showing the protein levels of GSK3-Beta which is predicted to be a target, in the higher expressing miR-199b-5p stable clone. [score:7]
F) As for E, showing GABRA6 and MATH3 proteins up-regulated after miR-199b expression, suggesting induction of differentiation. [score:6]
A) Representative data of a time course experiment of DAPT treatment of Daoy cell lines (6 h, 12 h, 24 h) with media supplemented and replaced every 4 h, and fold of expression of miR199b determined using quantitive real time detection, relative to time 0. B) Representative Western blot showing HES1 down-regulation after 12 h of induction of DAPT in the Daoy cell line. [score:6]
Indeed, two cell lines (Med8a and UW228) showed significant up-regulation of miR-199b-5p, thus supporting the hypothesis of epigenetic control of miR-199b-5p expression. [score:6]
Figure S2Mmu-miR-199b expression in mouse embryonic cerebellum and regulation of other potential targets by human miR-199b-5p. [score:6]
Figure S5Over -expression of endogenous miR199b upon DAPT treatment induces down-regulation of genes involved to embryonic stem cells and cancer stem cells in the Daoy cell line. [score:6]
We report here a novel level of regulation of HES1 expression that is driven by miR-199b-5p, which binds to the HES1 3′UTR and leads to unproductive translation. [score:6]
C) D283 and SH-SY5Y cells express similar levels of miR-199b-5p and miR-124a, with the latter known to be preferentially expressed in the central nervous system. [score:5]
Among the predicted targets for miR-199b-5p, which were obtained using two different algorithms (Text S1, Table S1), these genes were possible candidates related to the phenotype obtained after miR-199b over -expression. [score:5]
Correlation with survival for these patients with high levels of miR-199b expression showed a positive trend to better overall survival than for the low -expressing patients. [score:5]
In the ‘moderate low’ mo del, miR-199b-5p expression is lowered due to epigenetic control mechanisms, and then HES1 is over-expressed, leading to cell proliferation and induction of the SP and hence an increase in CD133+ cells. [score:5]
Overall, the picture of gene expression in our stable cell line over -expressing miR-199b-5p is in agreement with the phenotype that has been seen in the brain of the Hes1−/− mouse [23]. [score:5]
However, of note, the expression of PDGFR-B and SPARC, two genes recently correlated with metastatic MB [44], [45], is reduced in the presence of over -expression of miR-199b-5p, as we show in Text S1, Fig. S5D and describe in Text S1. [score:5]
C) Rapresentative mRNA expression of differentiation (e. g. MASH1, MATH3 and NEUROGENIN 2) and proliferation (e. g. c-MYC, CYCLIN D1) markers upon miR-199b-5p over -expression, as revealed by real-time PCR, comparing the stable 199bSC1 and 199bMC1 clones with empty vector clone. [score:5]
E–H) The effect of miR-199b-5p expression on the SP of Daoy cells is reversed by HES1 re -expression. [score:5]
I) Representative gene expression levels of the transgene miR-199b-5p in the tumor explant from mouse #5. The over -expression of miR-199b-5p was lost. [score:5]
Our approach started with a search for miRNAs (miRNA registry) with target genes involved in the Notch pathway, and we identified miR199b-5p as targeting HES1, the Notch effector. [score:5]
To determine the role of miR-199b-5p in MB cell biology, the miR-199b-5p expression construct was transfected into Daoy cells, and several stable clones over -expressing miR-199b-5p were selected. [score:5]
The Daoy stable clone with the empty vector (Ctl) and the Daoy stable clone over -expressing miR-199b-5p (199b) were transfected with a luciferase expression vector (Luc), generating, respectively, the Ctl-Luc#4 clone, and the199bLuc-1 and 199b-Luc-3 clones. [score:5]
The genes involved in stem cell biology selected for the study of their expression after over -expression of miR-199b-5p. [score:5]
These effects of miR-199b-5p on HES1 protein expression were not restricted to the stable clones or Daoy cells, as D283MED cells transiently transfected with the expression construct for miR-199b-5p also showed reduced HES1 levels (Text S1, Fig. S1B). [score:5]
The clones obtained were tested for luciferase expression levels and also validated for retention of the parental phenotype, in terms of both HES1 and miR-199b-5p expression (see Text S1, Fig. S4A–D). [score:5]
Left side: Under conditions of induced miR-199b-5p expression (1), the levels of HES1 decrease, relieving the inhibition on the neurogenic bHLHs (2). [score:5]
In the subset of patients where follow-up information was available (n = 45), the survival curve for the patients who expressed miR-199b at high levels showed a positive trend, with better overall survival than the low -expressing patients. [score:5]
In our ‘moderate high’ mo del, an increase in miR-199b-5p expression represses HES1, which then leads to an increase in pro-neural bHLHs gene expression, driving the cell towards differentiation processes. [score:5]
Further studies need to be performed to identify this tuned regulation mechanism of action through epigenetic inactivation of miR199b-5p expression during tumor development. [score:5]
The distribution of miR-199b-5p expression between non-metastatic (M0) and metastatic (M1, M2 and M3) cases showed that miR-199b-5p expression in the non-metastatic cases was significantly higher than in the metastatic cases (P = 0.001, Pearson Chi-Square test; Fig. 6B). [score:5]
To determine whether miR-199b-5p is effectively expressed in healthy human pediatric cerebella, we used 13 control samples obtained from the NICHD Brain and Tissue Bank for Developmental Disorders, at the University of Maryland, USA. [score:4]
These data showing the down-regulation of miR-199b-5p in metastatic MBs suggest a potential silencing mechanism through epigenetic or genetic alterations. [score:4]
Here, HES1 levels were restored, suggesting 2-OM block of HES1 repression by miR-199b-5p, providing further confirmation that miR-199b-5p targets HES1 directly. [score:4]
Table S3Stem and cancer stem genes, and genes associated with MB tumor development in Daoy cell lines over -expressing endogenous miR-199b-5p under treatment with DAPT. [score:4]
We show that miR-199b-5p expression is lost in metastatic patients and postulate a mechanism of regulation following epigenetic silencing through methylation processes occurring during carcinogenesis, identifying a new molecular marker for a poor-risk class in patients with MB. [score:4]
As illustrated in our mo del (Fig. 6E), we picture two different expression levels of miR-199b-5p in M0 and M+ patients, which might be due to epigenetic regulation during carcinogenesis. [score:4]
In a screening of MB cell lines, the miRNA miR-199b-5p was seen to be a regulator of the Notch pathway through its targeting of the transcription factor HES1. [score:4]
MiR-199b-5p over -expression blocks expression of several cancer stem-cell genes, impairs the engrafting potential of MB cells in the cerebellum of athymic/nude mice, and of particular interest, decreases the MB stem-cell-like (CD133+) subpopulation of cells. [score:4]
B) Quantification of decrease in mmu-miR-199b expression during mouse development and differentiation of the cerebellum. [score:4]
Overall, these data indicate a beneficial effect of over -expression of miR199b-5p, as a negative regulator of tumor growth of MB cells in this orthotopic xenograft nude-mouse mo del. [score:4]
Furthermore, two cell lines (Med8a and UW228) showed significant up-regulation of miR-199b-5p upon treatment. [score:4]
Recently it has also been shown that miR-199a*, which has the same sequence as miR-199b-5p, is involved in caspase activation by potentially acting through Met proto-oncogene down-regulation [42]. [score:4]
We focused on miR-199b-5p due to its ability to decrease HES1 expression under transient over -expression, as compared to miR-199a-5p (Text S1, Fig. S1A, B). [score:4]
The reason why some of the MB cell lines do not respond to the treatment with increasing miR-199b could be due to genetic loss of the gene itself, or to a strict cell-type regulation of miR-199b expression, reflecting the different origins of the cell lines. [score:4]
There was a significant decrease in HES1 protein levels, as revealed using an anti-HES1 polyclonal antibody; the decrease was also revealed by densitometry analysis (G; right panel) H) A 2′-O-methyl-oligoribonucleotide (2-OM) directed against miR-199b-5p was transfected into the stable 199bSC1 clone, with a representative Western blot and the quantification by densitometric analysis showing restored HES1 expression. [score:4]
Upon induction of de-methylation using 5-aza-deoxycytidine, lower miR-199b-5p expression was seen in a panel of MB cell lines, supported an epigenetic mechanism of regulation. [score:4]
These data showing down-regulation of miR-199b-5p in metastatic MBs indicates a mechanism of silencing through epigenetic or genetic alterations. [score:4]
Figure S4 Creation of bioluminescent Daoy cells over -expressing miR-199b-5p for in-vivo studies. [score:3]
The luciferase from the wild-type 3′UTR activity was reduced by 50% with miR-199b-5p expression, while 2′-O-methyl-oligoribonucleotide (2-OM; 400 nM) blocks this effect. [score:3]
We provide here evidence for the use of miRNAs in the clinic, with our anti-tumour therapy targeting of cancer stem cells by miR-199b-5p. [score:3]
A) Xenograft experiment over nine weeks, following s. c. injection of five mice with control Daoy cells (CTR side) and Daoy cells over -expressing miR-199b-5p (199b side). [score:3]
C) Kaplan-Meier survival estimates comparing patients with low versus high (relative to median) levels of miR-199b-5p expression (45 patients with available follow-up data). [score:3]
Right side: Under conditions of low miR-199b-5p expression, the levels of HES1 are higher (1), repressing the pro-neural bHLH genes, with a consequent increase in proliferation, SP and an enlargement of the CD133+ compartment (4). [score:3]
B) Representative Western blot from transient transfection of D283 cells with the expression construct for miR-199b-5p and using an empty vector. [score:3]
Decreased tumorigenicity of Daoy cells over -expressing miR-199b-5p. [score:3]
In our analysis of 61 patients with MB, the expression of miR-199b-5p in the non-metastatic cases was significantly higher than in the metastatic cases (P = 0.001). [score:3]
With this scenario, miR-199b-5p can be seen as part of the complex Notch signal-transduction pathway, as a fine tuner of the levels of expression of the HES1 bHLH transcription factor. [score:3]
MiRanda and Pita algorithms were applied to the selected “cancer-related” miR-199b-5p targets. [score:3]
Restored HES1 expression also reversed the effects of miR-199b-5p on cell proliferation (Fig. 3B). [score:3]
To determine whether miR-199b-5p expression has a role in human MB, samples from a cohort of 61 MB patients were analysed (see Experimental Procedures). [score:3]
We thus tested expression of miR-199b-5p by real-time PCR in a panel of MB cell lines following induction of de-methylation with 5-aza-deoxycytidine (Fig. 6D). [score:3]
The 199b-Luc1 and Ctl-Luc#4 clones where used for the in-vivo studies, with the data shown as means±SD from two independent experiments C) Representative data of the expression of miR-199b-5p in the luciferase clones, relative to the luciferase clone carrying the empty vector. [score:3]
The whole patient population (n = 61) was then divided into two groups, as low versus high miR-199b-5p expression, based on the overall median. [score:3]
MiR-199b-5p over -expression lowered the levels of the endogenous HES1 protein; in contrast, miR-199a induced an increase in HES1 levels 48 h after transfection. [score:3]
A) Mmu-miR-199b in situ mRNA expression is detectable at E14.5 and in newborn mouse (p0) cerebellum. [score:3]
As shown in Fig. 6 and Text S1, Table S2, we show great variability in the miR-199b-5p expression levels, which might be due to genetic chromosomal alterations or epigenetic silencing in a subset of patients with worse outcome. [score:3]
Expression of miR-199b-5p in human medulloblastoma tumors. [score:3]
A) In-vivo bioluminescence analyses using IVIS 3D of 199b-Luc1 mouse xenografted with Daoy Luc1 cell line overexpressing miR-199b by stable clone analyses. [score:3]
Table S1 Cancer related targets of miR-199b-5p. [score:3]
This prevents activation of the Notch response (see Text S1, Materials), thus blocking the presenilin-secretase complex and enhancing miR199b-5p expression [50], [51]. [score:3]
HES1 over -expression rescues the miR-199b-5p clone phenotype. [score:3]
Over -expression of miR-199b-5p reduces cell proliferation and impairs the clonogenic potential of MB cell lines. [score:3]
This was opposite to the effects seen in the stable 199bSC1 clone over -expressing miR-199b-5p (see Fig. 1C and Fig. 3C). [score:3]
Despite the correlation with M status, the over -expression of miR-199b-5p did not lead to a decrease in cell motility of Daoy cells (Text S1, Fig. S2E). [score:3]
Indeed loss of Cyclin D1 in over -expressing miR-199b-5p clones are a reminder of the similar effects seen in Ccnd1–/– mice, which have decreased early GNP proliferation and early ataxia as a consequence of a delay in acquiring normal cerebellar function, thus affecting progression of the pre-neoplastic lesions to MBs [43]. [score:3]
E–F) Luciferase activity from a reporter vector containing wild-type HES1 3′UTR and HES1 3′UTR mutated in the miR-199b binding site, co -transfected or not with an expression vector for miR-199b-5p. [score:3]
Again, miR-199b-5p over -expression lowered the levels of the endogenous HES1 protein. [score:3]
MiR199b-5p expression specifically impairs the cancer-stem-cell (CD133+) population, which results in vivo in impairment of MB tumor development in the cerebellum xenograft mouse mo del, thus providing proof of concept. [score:3]
This effect of miR-199b-5p over -expression was reduced by 2-OM transfection (pink squares). [score:3]
A) Box-plot of expression levels of miR-199b-5p in healthy human cerebella in the two age ranges indicated. [score:3]
0004998.g006 Figure 6A) Box-plot of expression levels of miR-199b-5p in healthy human cerebella in the two age ranges indicated. [score:3]
The findings here indicated that miR-199b-5p is a potential inhibitor of tumor formation. [score:3]
GSK3-Beta levels were not down-regulated, and were instead slightly increased, as is clear from the quantification by densitometric analysis shown in the right panel, where the data shown are means±SD from two independent experiments, each carried out in triplicate D) MiR-199b-5p is predicted to bind other UTRs (see Supporting Table S1). [score:3]
Hsa-miR-199b-5p silences HES1 expression via 3′UTR binding. [score:3]
M0 and M+ patients show different expression levels of miR-199b-5p, which could be driven by an epigenetic mechanism. [score:3]
Here we show that miR-199b-5p expression correlates with metastasis spread, identifying a new molecular marker for a poor-risk class in patients with MB. [score:3]
Expression levels of miR199b in human cerebellum and in tumors, and the correlation with prognosis. [score:3]
Both miR-199b-5p stable clones showed increases in expression of pro-neural bHLH. [score:3]
The data shown are means±SD from two independent experiments, each carried out in triplicate G) Silencing of endogenous expression of miR-199b-5p via transfection of a 2-O-methyl oligoribonucleotide antisense (2-OM-a) leads to an increase in Daoy cells proliferation, probably relieving the control of endogenous miR-199b-5p on HES1 3′UTR. [score:3]
The effects of miR-199b-5p over -expression are reversed by HES1 transfection. [score:3]
The analysis of the over -expressing miR-199b-5p clones suggested that miR-199b-5p can impair the proliferation and engrafting potential of MB cells. [score:3]
In the light of our data on the regulation of the Notch pathway via miR-199b-5p modulation, it will be of interest to focus future studies on the role of Notch-regulated genes in metastatic MB patients. [score:3]
0004998.g004 Figure 4A) Xenograft experiment over nine weeks, following s. c. injection of five mice with control Daoy cells (CTR side) and Daoy cells over -expressing miR-199b-5p (199b side). [score:3]
Figure S1 A) Representative Western blots from transient transfection of HEK293 cells with expression constructs for miR-199b-5p and miR-199a. [score:3]
The Daoy cells showed a 5.2% fraction of SP cells, while the stable 199bSC1 and 199bMC1 clones over -expressing miR-199b-5p do not show significant levels of SP cells (0.2%, 0.4%, respectively) (8.54 MB TIF) Click here for additional data file. [score:3]
HEK-293 cells were then transfected with the relative luciferase activity showing that miR-199b-5p co-transfection decreased reporter gene activity, thus indicating binding with the 3′UTR and destabilisation of productive translation of luciferase mRNA (Text S1, Fig. S1E). [score:3]
Over -expression of miR-199b-5p decreases the CD133+ compartment of Daoy cells. [score:3]
D) MiR-199b-5p expression by real-time PCR in a panel of five MB cell lines untreated or treated with 5-Aza-C (DAC−/+); the de-methylation induced miR-199b-5p transcription in two cell lines: Med8a and UW228. [score:3]
In the present study, we have identified a mechanism of HES1 gene regulation via the miRNA miR-199b-5p. [score:2]
In columns, ID of material, age in year and relative expression of miR-199b-5p compared to the level of (U6) and 2 [−Delta] Ct values. [score:2]
B) MiR-199b-5p highly expressing cases are mostly M0 P = 0.001 (Pearson Chi-Square test). [score:2]
F) Proliferation assay (MTS) of D283MED and ONS76 cells over -expressing miR-199b-5p after transient transfections, as indicated. [score:2]
MiR-199b-5p showed greater expression in the explants from the younger healthy controls (Mann-Whitney test, P = 0.006). [score:2]
This thus demonstrated a role for miR-199b-5p in negative regulation of this fraction of tumor-initiating cells. [score:2]
MiR-199b-5p showed higher expression in explants from younger controls (Mann-Whitney test, P = 0.006). [score:2]
A) In columns Age at diagnosis in month, Follow-up time in months, State at last news, Mestatasis (M) stage, Histology, Relative expression of miR-199b-5p compared to the level of (U6) and 2 [−Delta] Ct values. [score:2]
MiR-199b-5p effects on the 3′UTR of its putative target gene, HES1. [score:2]
We thus examined the influence of miR-199b-5p on the population of tumor cells that exclude the Hoechst 33342 dye, a strategy to identify these SP cells. [score:1]
0004998.g001 Figure 1 In-vitro function of miR199b-5b on proliferation and differentiation of Daoy MB cells. [score:1]
Here, we envisage the use and delivery of miR199b-5p in situ into the cerebellum of MB-affected children under 3 years of age (and positive to HES1), to thus impair the maintenance of the tumor-initiating CD133+ cancer cells. [score:1]
Here miR-199b-5p can influence this side population and the CD133+ population of Daoy cells, namely the cancer stem cells. [score:1]
We measured miR-199b-5p expression, comparing five cerebellum samples obtained from 0–1-year-old children with six from 13–16-year-old children (Fig. 6A). [score:1]
Other potential targets of miR-199b-5p were also investigated in this way (Text S1, Fig. S2C, D). [score:1]
There is no effect with the miR-199b-5p together with the HES1 3′UTR mutated in the binding site. [score:1]
While the effects of miR-199b-5p could be explained by triggering of apoptosis, our cytofluorimetric assays suggested that impairment of MB cell proliferation is not linked to extensive apoptosis of cells over -expressing miR-199b-5p (see cell cycle assay on Fig. 1A). [score:1]
The effects of miR-199b-specific 2-OM were also confirmed in wild-type Daoy cells, where it potentially acts on the endogenous miR-199b (Text S1, Fig. S2G). [score:1]
In contrast, the D283Med cells showed considerably lower levels of miR-199b-5p. [score:1]
Figure S3 FACS analysis for the role of miR-199b-5p on the Daoy cell side population. [score:1]
MiR-199b-5p depletes the side population compartment in the Daoy cell line, and negatively regulates MB tumor stem-cell populations. [score:1]
Therefore, to investigate the role of miR-199b-5p in an in vivo tumor mo del, we stabilized the 199bSC1 and control Daoy clones with an expression vector carrying luciferase cDNA. [score:1]
Infection with MB cells in an induced xenograft mo del in the mouse cerebellum and the use of an adenovirus carrying miR-199b-5p indicate a clinical benefit through this negative influence of miR-199b-5p on tumor growth and on the subset of MB stem-cell-like cells, providing further proof of concept. [score:1]
MiR-199a* (also known as miR-199a-5p, and with an identical sequence to miR-199b-5p) is also reduced in hepatocellular carcinoma [30]– [32]. [score:1]
As controls, HES1 3′UTR mutated in the miR-199b-5p binding site was not affected by miR-199b-5p (Text S1, Fig. S1E), and when a 2-O′-methyl oligoribonucleotide (2-OM) complementary to mature miR-199b-5p was co -transfected, it counteracted the effects of miR-199b-5p transfection, restoring reporter activity (Text S1, Fig. S1E). [score:1]
After nine weeks, four out of the five mice showed statistically significant differences in these bioluminescence signals between control sides and miR-199b-5p counter sides (Fig. 4C). [score:1]
The correlation that we show between miR-199b-5p and tumor M stage indicates that miR-199b-5p expression levels can be investigated concomitant with tumor resection. [score:1]
E) The interplay between miR-199b-5p and the Notch pathway. [score:1]
G–I) Pre-miR-199 was cloned and transfected into Daoy cells, and three stable clones were evaluated for HES1 expression by qRT PCR and Western blotting. [score:1]
Overall, a significant difference in tumor volumes between control flanks and miR-199b-5p flanks was seen (Fig. 4A). [score:1]
To strengthen these findings, the 199bSC1 clone was transfected with 2-OM antisense to miR-199b-5p and used as a negative control (Text S1, Fig. S1I). [score:1]
The xenograft tumors from mouse #5 and mouse #4 were explanted and analyzed for miR-199b-5p and HES1 expression and evaluated histopathologically (Text S1, Fig. S4E–H). [score:1]
D) Photon emission of 3 mice injected in the fourth ventricle with respectively: 199bLuc-1, Ctl-Luc-4 infected with mock AdV5, and Ctl-Luc-4 infected with a miR-199b-5p AdV5. [score:1]
Of note, when analyzed according to the Pita algorithm, the value of ΔΔG for the binding of miR-199b-5p to the 3′UTR of GSK3-β is very high, indicating poor accessibility to the 3′UTR [41] (see Text S1, Table S1). [score:1]
MiR-199b-5p and miR-199a-5p were the better scoring miRNAs, and were predicted to bind the 3′UTR of human bHLH HES1. [score:1]
We further show that in a xenograft mo del, MB tumor burden can be reduced, indicating the use of miR199b-5p as an adjuvant therapy after surgery, in combination with radiation and chemotherapy, for the improvement of anti-cancer MB therapies and patient quality of life. [score:1]
Taken together, these data show that miR-199b-5p can impair tumor formation in vivo in athymic nude/nude mice. [score:1]
As further confirmation of these effects, we also injected the CTL cells infected with an adenovirus coding for miR-199b-5p: in agreement with the previous findings, these mice also showed reduced BLI after 4 weeks (Fig. 4F). [score:1]
In-vitro function of miR199b-5b on proliferation and differentiation of Daoy MB cells. [score:1]
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[+] score: 156
Atrasentan up-regulated miR-199b-5p expression, down-regulated klotho expression, and increased the antioxidant ability of HK-2 cells exposed to a high concentration of glucose. [score:11]
To further demonstrate the relationship between miR-199b-5p and klotho, the HK-2 cells were transfected with a miR-199b-5p mimic or inhibitor to overexpress or down-regulate the expression of miR-199b-5p (Fig. 5A,E). [score:10]
However, when cells were co-incubated with the histone deacetylase inhibitor Trichostatin A (TSA), miR-199b-5p expression levels were up-regulated at higher levels (Fig. 4A). [score:8]
org data bank and that the activation of miR-199b-5p inhibited the 3′ UTR activity of klotho and down-regulated its expression level in HK-2 cells. [score:8]
MiR-199b-5p also targeted klotho and down-regulated its expression, illustrating a potential mechanism for the protective effect of atrasentan against renal tubular injury in DN. [score:7]
A luciferase reporter assay showed that the miR-199b-5p mimic significantly decreased the 3′ UTR activity of klotho (Fig. 5B) and inhibited its expression (Fig. 5C,D), whereas the miR-199b-5p inhibitor had the opposite effects (Fig. 5F–H). [score:6]
miR-199b-5p targeted klotho and regulated its expression in HK-2 cells. [score:6]
Atrasentan improved renal function, decreased miR-199b-5p expression, and increased klotho expression in STZ -induced DN mice. [score:5]
Increased miR-199b-5p expression (Fig. 3A) and decreased klotho expression (Fig. 3B) were observed in the HK-2 cells exposed to a high concentration (20 mmol/L) of glucose. [score:5]
The HK-2 cells were transfected with an miR-199b-5p mimic/inhibitor or NC, and the expression of miR-199b-5p was quantified by real-time PCR (A,E). [score:5]
Recently, He et al. found that klotho was a target gene of miR-199a-5p in cancer 18, suggesting that the miR-199 family may be involved in the regulation of klotho in DN. [score:4]
Atrasentan led to a decrease in histone acetylation, suggesting one possible mechanism by which it may down-regulate miR-199b-5p. [score:4]
In current study, we focused on the function of miR-199b-5p in the regulation of klotho expression in renal tubular injury of DN. [score:4]
The HK-2 cells were exposed to various concentrations of TSA (0.1, 0.5 and 1.0 μmol/L) for 72 h and the expression of miR-199b-5p was then quantified by real-time PCR (A). [score:3]
org database, klotho is a potential target of miR-199b-5p (Suppl. [score:3]
Atrasentan altered the expression of miR-199b-5p and klotho and the antioxidant ability of HK-2 cells. [score:3]
Administrated cells with methylase 5′-Aza-dC, no alteration of miR-199b-5p expression was observed (data not shown). [score:3]
U6 and β-actin served as control genes to normalize the expression of miR-199b-5p and klotho, respectively. [score:3]
Real-time PCR was used to detect serum and renal tubular epithelial cell miR-199-5p expression (D). [score:3]
miR-199b-5p participated in the effects of atrasentan on the expression of klotho, antioxidant activities, and caspase activity of HK-2 cells. [score:3]
Atrasentan altered the miR-199b-5p and klotho expression levels of STZ -induced DN mice. [score:3]
The miR-199b-5p mimic reversed the atrasentan -induced increase in the expression of klotho (Fig. 6A). [score:3]
We also found that miR-199b-5p targeted klotho at two binding sites using the MicroRNA. [score:3]
The expression levels of miR-199b-5p and klotho were assessed with a real-time PCR system (Applied Biosystems 7900 Fast Real-Time PCR System, USA) with Power SYBR® Green PCR Master Mix (Applied Biosystems, USA). [score:3]
How to cite this article: Kang, W. -L. and Xu, G. -S. Atrasentan increased the expression of klotho by mediating miR-199b-5p and prevented renal tubular injury in diabetic nephropathy. [score:3]
In the present study, high glucose (20 mmol/L) significantly increased the expression level of miR-199b-5p in HK-2 cells. [score:3]
Interestingly, the effects of the miR-199b-5p mimic on klotho expression, antioxidant ability, and caspase-3 activity were all dramatically reversed in the HK-2 cells treated with 20 mmol/L glucose. [score:3]
The expression of miR-199b-5p was quantified by real-time PCR (A). [score:3]
As shown in Fig. 7, overexpressed miR-199b-5p resulted in an increase in renal function parameters such as urinary albumin/creatinine, serum BUN, serum creatinine, urinary KIM-1, urinary NGAL and urinary NAG (Fig. 7A–F). [score:3]
Fluorescence quantitative PCR of cDNA was performed with primers specific for miR-199b-5p and klotho expression. [score:2]
The mice treated with atrasentan were also injected intravenously with AAV- miR-199b-5p (with or without 20 mg/kg klotho by intraperitoneal injection) or a control vector twice per week for 8 weeks. [score:1]
As shown in Table 2, the serum miR-199b-5p level was negatively related to serum BUN, creatinine, and klotho concentrations. [score:1]
3.6 The effects of miR-199b-5p and klotho on renal function in vivo. [score:1]
Atrasentan altered the epigenetic modification of the miR-199b-5p promoter in HK-2 cells. [score:1]
Atrasentan decreased histone deacetylation of the miR-199b-5p promoter in HK-2 cells exposed to high glucose. [score:1]
The increase in the level of klotho, mediated by miR-199b-5p, may be a possible mechanism by which atrasentan prevents renal tubular injury in DN. [score:1]
Serum miR-199b-5p levels were significantly decreased in the subjects with abnormal albuminuria and the highest level was in the macroalbuminuric subjects. [score:1]
The relative expression levels of miR-199b-5p and klotho were calculated with the 2 [−ΔΔCT] method. [score:1]
To investigate the effects of miR-199b-5p and klotho on renal function in vivo, the STZ -induced diabetic mice were injected with AAV-miR-199b-5p to overexpress miR-199-5b. [score:1]
The miR-199b-5p mimic also canceled the elevated activities of the antioxidant indicators (T-AOC, SOD, and CAT, and GSH) and the reduced caspase-3 activity induced by atrasentan (Fig. 6B–F). [score:1]
Importantly, we found that high glucose enhanced histone H3, but not H4, binding to the miR-199b-5p promoter and that atrasentan markedly weakened this binding. [score:1]
Univariate correlations with serum miR-199b-5p level were also performed. [score:1]
In addition, Fragments of the 3′ UTR of klotho containing putative miR-199b-5p binding sites were amplified by PCR technology and then cloned into pMIR- RB-REPORTTM vectors (Guangzhou RiboBio Co. [score:1]
As expected, the additional injection of klotho reversed the negative effects of AAV-miR-199b-5p on renal function in vivo. [score:1]
The effects of miR-199b-5p and klotho on the renal function of STZ -induced DN mice. [score:1]
We observed that high glucose increased histone H3 acetylation in the miR-199b-5p promoter region, which led to the activation of this miRNA. [score:1]
The effects of miR-199b-5p and klotho on renal function in vivoTo investigate the effects of miR-199b-5p and klotho on renal function in vivo, the STZ -induced diabetic mice were injected with AAV-miR-199b-5p to overexpress miR-199-5b. [score:1]
Univariate correlations with serum miR-199b-5p levels concentrations. [score:1]
An AAV-miR-199b-5p/empty vector, with or without 20 mg/kg of klotho by intraperitoneal injection, was intravenously injected into the mice twice every week for 8 weeks. [score:1]
An miR-199b-5p mimic (100 mmol) or an NC was then transfected into the cells. [score:1]
In STZ induced diabetics mice, additional injection of klotho reversed the negative effects of AAV-miR-199b-5p on renal function. [score:1]
The constructs were then co -transfected with pre-mir-199b-5p or a negative control (NC) with Lipofectamine2000 (Invitrogen, USA) according to the manufacturer’s recommendations. [score:1]
The epigenetic modification of the miR-199b-5p promoter was explored in HK-2 cells. [score:1]
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[+] score: 154
Since virtually 100% HCCs exhibit a strong down-regulation of miR-199 which is instead expressed at substantial level in normal hepatocytes, where it represents the third most highly expressed miRNA [48], this virus was designed to prevent cytolytic activity in healthy cells, thereby addressing the important issue of a novel therapeutic approach with improved efficacy and safety in HCC. [score:8]
This evidence confirms that miR-199, constitutively expressed in HepG2/199 cells, can control E1A expression by targeting the homologous sequences places downstream of the adenoviral E1A gene. [score:7]
TaqMan, Real Time PCR analysis showed that miR-199 expression was significantly increased in the HepG2/199 cell line in comparison with the basal expression level in the HepG2 cells (p-value = 0.0005) and not significantly different from human normal liver (NL) expression levels (p-value = 0.06). [score:7]
The inhibition of E1A mRNA and protein was demonstrated in miR-199 expressing HepG2 cells, while E1A normal expression could be detected in HepG2 wild type cells (Figure 2A-B ). [score:7]
The rationale of the work was based on the differential expression of miR-199 between normal versus cancer liver cells and in particular on the basis that miR-199 is down-regulated in human hepatocellular carcinoma [12]. [score:6]
To verify if miR-199 could regulate viral replication in vitro, Ad-199T and Ad-Control were used to infect two different cell lines: (1) HepG2, derived from human liver carcinoma and not expressing miR-199; (2) HepG2/199, which derives from HepG2 cells engineered to constitutively express miR-199a (Figure S3 ). [score:6]
To produce stable cell clones expressing miR199, HepG2 cells were transfected with 2 µg of a miR-199 expressing plasmid, pIRES-miR199, using Lipofectamine 2000 (Invitrogen, Carlsbad, CA). [score:5]
This objective was achieved by introducing into the viral genome multiple miR-199 target sites able to modulate the expression of the E1A gene. [score:5]
Quantitative PCR revealed that miR-199 was down-regulated in tumors in comparison with normal liver (p value = 0.0146) (Figure 8E ). [score:4]
In particular, miR-199 was reported to be consistently down-regulated in HCC [12]. [score:4]
Useful for the objective of this study, we previously showed that miR-199 is down-regulated in liver tumors arising in this mo del. [score:4]
The involvement of miR-199 in the pathogenesis of HCC was linked to the abnormal regulation of multiple target genes, such as mTOR, c-Met, HIF-1α and CD44 [13, 14, 15, 16]. [score:4]
This mouse strain has an increased susceptibility to the carcinogen diethylnitrosammine (DEN) and tumors exhibit a miRNA profile similar to human HCC, including the down-regulation of miR-199. [score:4]
This latter vector was used as recipient of the miR-199 targeting site (199T) into the MluI restriction site, to generate the pENTR_E1A/199T/E1B vector. [score:3]
As expected, the luciferase activity was significantly decreased only in samples co -transfected with miR-199 (p value = 0.007), thus proving the functional interaction between miR-199 and the artificial target sequences (Figure S1 ). [score:3]
By investigating in vitro and in vivo properties of Ad-199T, we demonstrated that this CRAd could replicate very poorly in cells expressing miR-199, while its replication could proceed regularly in cells lacking the expression of this miRNA. [score:3]
HepG2/199 cell line stably express miR-199. [score:3]
For the construction of the adenoviral miR-199 dependent plasmid, an MluI fragment containing the microRNA-199 target sequence was amplified by PCR from the plasmid pGL3-199T and inserted into a MluI site located in the 3’ UTR of E1A sequence in the vector pENTR_E1A/E1B, to generate pENTR_E1A/199T/E1B. [score:3]
E1A expression is miR-199 dependent. [score:3]
0073964.g002 Figure 2To assess the expression of E1A in presence or absence of miR-199, 7×10 [4] cells of HepG2 and HepG2/199 cell lines were seeded and infected with 1x10 [6] I. U. of Ad-199T or with 1x10 [6] I. U. of Ad-Control and harvested after 48 hours. [score:3]
A replicative control adenovirus, Ad-Control, without miR-199 target sequences, was also developed (Figure 1 ). [score:3]
This work establishes that the presence of miR-199 target sites within the 3’ UTR of E1A gene represents a strategy to generate recombinant adenoviruses with significant oncolytic activity against liver cancer, which exhibits low level of miR-199, coupled with reduced hepatoxicity. [score:3]
This foreseeable finding was a consequence of the inhibitory effect imposed by miR-199 on Ad-199T replication, thereby preventing its lytic activity in healthy cells. [score:3]
To assess if these findings were related to miR-199 expression, we analyzed the level of the miRNA in normal liver and tumor tissues. [score:3]
First, in 3 days old mice, which have a limited or absent immune response [49], Ad-199T was not able to replicate in the liver while an identical control virus, lacking the miR-199 target sites, could efficiently undergo several rounds of replication. [score:3]
A progressive accumulation of viral DNA in the HepG2 cells infected with Ad-199T indicates that active viral replication is efficiently occurring in this cell line; on the contrary, in HepG2/199 cells infected with Ad-199T the viral DNA did not increase over time, confirming that the virus replication was inhibited by the presence of miR-199. [score:3]
Figure S9(A) To asses miR-199 expression levels in Hep3B cell line, a TaqMan, Real Time PCR was performed. [score:3]
The present work is the first that make use of miR-199 to target an oncolytic virus to cancer cells in vivo. [score:3]
The results showed that Hep3B displayed a very low basal miR-199 expression level, even lower than HepG2 cells. [score:3]
To confirm its functional activity, we first cloned the miR-199 artificial target sequence downstream of the firefly luciferase reporter gene at the XbaI restriction site within the pGL3 vector (Promega, Madison, WI, USA), to generate pGL3/199T vector. [score:3]
Figure S3 The pIRES-miR199 vector, expressing miR-199, was stably transfected in the hepatocellular carcinoma derived cell line HepG2, generating the HepG2/199 cell line. [score:3]
Since miR-199 is instead expressed at variable but significant level in any normal tissues, Ad-199T could lack toxicity in tissues other than liver as well. [score:3]
Since miR-199 is highly expressed in normal liver, but not in HCC, this virus seems to be well suited for the treatment of liver cancer. [score:3]
To assess replication properties of Ad-199T in vivo, we tested its ability to replicate in the liver of B6D2 wild type mice, where miR-199 is constitutively expressed. [score:3]
The MluI site was used for introducing the miR-199 target segment, originally cloned into the pGL3/199T (as described above). [score:3]
To assess the expression of E1A in presence or absence of miR-199, 7×10 [4] cells of HepG2 and HepG2/199 cell lines were seeded and infected with 1x10 [6] I. U. of Ad-199T or with 1x10 [6] I. U. of Ad-Control and harvested after 48 hours. [score:3]
miR-199 directly interacts with its target sequence cloned in the pGL3/199T vector, as evaluated by luciferase activity in Hep3B cells. [score:2]
These results established that viral replication of Ad-199T was indeed miR-199 -dependent in vitro. [score:1]
Four copies of a 22 bp DNA segment complementary to miR199 were inserted within the 3’-untraslated region (3’-UTR) of the E1A gene, which is essential for adenoviral replication. [score:1]
To develop a conditionally replication-competent oncolytic adenovirus (CRAd) under miR-199 control, named Ad-199T, four copies of a 22 bp DNA segment complementary to human and mouse miR-199, were inserted within the 3’-untraslated region (3’-UTR) of the E1A gene, essential for adenoviral replication. [score:1]
Here, to improve tumor specificity and reduce toxicity for normal cells, we developed a novel CRAd whose replication was controlled by miR-199. [score:1]
This vector was transfected into the hepatocarcinoma Hep3B cells together with either miR-199 or scrambled oligos. [score:1]
These results demonstrated that Ad-Control replicates efficiently in normal liver cells, inducing hepatotoxicity, while miR-199 could control Ad-199T lytic cycle in normal hepatocytes in vivo. [score:1]
This evidence confirms that miR-199 could control Ad-199T replication in normal liver cells in vivo. [score:1]
Taken together, these findings can be interpreted as evidence that Ad-199T could replicate more efficiently in tumor tissues, where it can produce cytolysis, and this property was most likely miR-199 -dependent. [score:1]
Here, we took advantage of this information to produce a new type of CRAd able to replicate only in cells lacking miR-199, with the aim of making viral replication and cytolytic effect specifically selective for HCC cells. [score:1]
The Ad-199T virus was designed to replicate in miR-199 -negative cells. [score:1]
miR-199 controls Ad-199T replication in vivo. [score:1]
miR-199 controls Ad-199T replication in vitro. [score:1]
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[+] score: 32
These data confirm that miR-181a and b, miR-9, miR-204, miR-135a, and miR-199b target endogenous SIRT1 and downregulate its expression. [score:8]
Therefore, expression of select miRNAs, including the miR-199 and miR-30 families, decreases during reprogramming and may allow for the upregulation of SIRT1 protein expression. [score:8]
This correlated with the downregulation of miR-199 andmiR-30 families that target SIRT1 (Figure 6C). [score:6]
miR-181a and b, miR-9, miR-204, miR-135a, and miR-199b target endogenous SIRT1. [score:3]
Specifically, SIRT1 expression is repressed by miR-181a and b, miR-9, miR-204, miR-135a, and miR-199b. [score:3]
Overexpression of miR-181a and b, miR-9, miR-204, miR-135a, and miR-199b decreased SIRT1 protein levels in mESCs (Figure 4B). [score:3]
miR-199 is highly expres-sed in mouse embryonic fibroblasts and skin. [score:1]
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[+] score: 23
Finally, the increase in miR199-3p may ultimately offset the P53 upregulation in heart failure. [score:4]
Research has suggested that miR199 may have significant differential expression in the myocardium during heart failure. [score:3]
We performed rescue experiments by transfection with the combination of anti-miR199-3p and shRNA-CABLES1 in cardiac c-kit [+] cells and detected the protein expression by (Fig.   6a). [score:3]
Collectively, our findings uncover one new mechanism by which P53 induced miR199a-3p expression and, in turn, miR199-3p decreased P53 activity. [score:3]
We performed experiments by transfection with the combination of anti-miR199-3p and shRNA-CABLES1 in cardiac c-kit [+] cells and detected the P53 protein expression by (Fig.   6a). [score:3]
We further demonstrated that P53 induced miR199a-3p expression and, in turn, miR199-3p decreased P53 activity. [score:3]
The miR199 family plays an important role in hypoxia -induced cell death through regulation of hypoxia-inducible factor-1a (HIF-1a) and the stabilization of the proapoptotic factor p53 [9]. [score:2]
These assays demonstrated that P53 induced miR199a-3p expression and, in turn, miR199-3p decreased P53 activity. [score:2]
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[+] score: 20
Here, we found that the expression levels of miR-199 family members were up-regulated (3–4 fold) in the liver of S. japonicum-infected mice at 45 dpi compared with that of uninfected mice, indicating that dysregulation of miR-199 members may represent a general mechanism contributing to the fibrotic process. [score:6]
MiRNAs significantly dysregulated in the mid-phase of infection (dpi 30), such as mmu-miR-146b and mmu-miR-155, may relate to the regulation of hepatic inflammatory responses, whereas miRNAs exhibiting a peak expression in the late phase of infection (dpi 45), such as mmu-miR-223, mmu-miR-146a/b, mmu-miR-155, mmu-miR-34c, mmu-miR-199, and mmu-miR-134, may represent a molecular signature of the development of schistosomal hepatopathy. [score:6]
Further, Murakami et al. observed that the progression of liver fibrosis was related with over -expression of the miR-199 and 200 families in a CCL4 -induced murine mo del [41], and miR-199a-5p was also observed to mediate TGF-β -induced lung fibroblast activation by targeting Caveolin-1 [42]. [score:5]
In addition, some other miRNAs previously reported to be associated with fibrosis, such as miR-34c, miR-199, and miR-214, also exhibited a peak expression in the liver of infected mice at 45 dpi (Table 2 and Figure 3). [score:3]
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[+] score: 19
The expression of four miRNAs was only dependent on the PPARγ expression status of the animals; miR-199, miR-455 and miR-1192 were upregulated in mice with dominant -negative PPARγ irrespective of the diet given to the animals, the fourth, miR-592, was reduced in mutant animals (“a” in Fig. 5C). [score:8]
Among those, were miR-7a, miR-7b, miR-146b, miR-199a and miR-199b* that were regulated at very early time-points after induction of MSCs and show the same direction of up- or down-regulation in the NIH/3T3 mo del. [score:6]
Five of these eight miRNAs (miR-199a, miR-7, miR-146b, miR-7b, and miR-199b*) were similarly regulated early during the adipogenesis process of MSCs, indicating that their regulation was due to cell cycle arrest rather than adipogenesis. [score:3]
Members of 5 miRNA families were coordinately up regulated during adipogenesis, namely let-7a, let-7c, let7-e, let-7g, and let-7i; members of the miR-29 family miR-29a, miR-29b, and miR-29c; miR-30a_1, miR-30b, miR-30c, miR-30d, and miR-30e; miR-181a, and miR-181b; miR-199a, miR-199a-3p, miR199-b*. [score:2]
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[+] score: 16
From the miRNA database, we also observed that TWEAK down-regulates miRNAs that are targeting proliferation and remo deling of muscles (miR-107), matrix metalloprotease such as aggrecanase-2 (miR-192), adamtsl-3 (miR-199-3p), and genes involved in increasing cell growth and proliferation, and microtubule -associated proteins (miR-23b) (Table 3). [score:6]
Some of the important miRs with known/putative targets and differentially regulated by TWEAK are presented in Figure 3. Our results showed that TWEAK reduced the expression of muscle-specific miR-1, miR-133a, miR-133b and miR-206 in addition to several other miRs including miR-27, miR-23, miR-93, miR-199, miR-107, and miR-192 (Figure 3A). [score:6]
Low-density miRNA array of TWEAK -treated C2C12 myotubes showed down-regulation of miR-1, miR-133a, miR-133b, miR-206, miR-27, miR-23, miR-93, miR-199, miR-107, and miR-192. [score:4]
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[+] score: 14
List of the main miR-199a-5p predicted targets significantly downregulated following miR-199-5p overexpression in human fibroblasts using the bioinformatics tool miRonTop (http://www. [score:8]
The mean normalized fluorescence intensity for the agilent probe is displayed; (B) Western blot analysis showing the effect of miR-199-5p or miR-199a-3p overexpression in hFL1 lung fibroblasts on SMAD4 and αSMA expression. [score:5]
Moreover, our data indicated that miR-199a-3p had distinct effects on lung fibroblasts differentiation than miR-199-5p, as assessed by their different impact on αSMA (Figure S14B and data not shown). [score:1]
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[+] score: 14
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-151, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
In contrast, the miRNAs up-regulated in the liver (miR-199-3p, miR-199-5p, miR-21, miR-214 and miR-210) showed significantly higher levels in mouse serum at 12 weeks post infection (Fig. 2), however these failed to differentiate S. mansoni infected from uninfected humans (Fig. S4). [score:4]
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infectionBetween weeks 6 and 12, female parasites continue to produce ∼300 eggs per day [51], resulting in an increase in the number of granulomas in the liver and the development of fibrosis [45]. [score:4]
Temporal expression analysis of miR-199, miR-214, miR-21, miR-210, miR-122, miR-192 and miR-194 in the liver during S. mansoni infection. [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
The 5 host miRNAs were detectable in serum (miR-21, miR-199-3p, miR-199-5p, miR-210, miR-214) but showed variable abundance and failed to differentiate ‘egg -positive’ and ‘egg -negative’ participants (Fig. S4). [score:1]
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[+] score: 13
The relationship between expression level of miR-199 and 200 families and expression level of three fibrosis related genes. [score:5]
Figure S2Comparison of the expression level of miR-199 and 200 familes in several cell lines and human liver tissue. [score:3]
The expression level of miR-199 and 200 families in human liver biopsy specimen by real-time qPCR. [score:3]
The miR-199 and miR-200 families have are circumstantially related to liver fibrosis. [score:1]
The sequences of mmu-miR-199a-5p, mmu-miR-199b, mmu-miR-199b, mmu-miR-200a, and mmu-miR-200b in mouse miRNA corresponded to the sequences of hsa-miR-199a, hsa-miR-199a*, hsa-miR-199a, hsa-miR-200a, and hsa-miR-200b in human miRNA, respectively (Table S3). [score:1]
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[+] score: 13
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
MiR-206, miR-133, miR-199, miR-100 and miR-195 were implicated in the autophagy pathway targeting BCL2, MTOR and SQSTM1 as possible autophagy gene targets (Table 6). [score:5]
However, miR-199 (p value = 0.01) and miR-200 (p value = 0.004) in contrary to the microarray results were significantly upregulated in cbs [+/–] in comparison with the control cbs [+/+] (p value < 0.05). [score:4]
MiRNAs (miR-199 and miR-200) were significantly upregulated in cbs [+/–] in comparison with the control ([*] p < 0.05, [**] p < 0.01). [score:4]
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[+] score: 13
Adenovirus -mediated p300 expression significantly increased levels of all cluster members including miR-20a (1.95-fold ±0.03, p<0.0001, Figures 4C and D), while expression of an unrelated miRNA, miR-199, was unchanged (Figure 4D), confirming that p300 gain can positively regulate expression of this anti-angiogenic microRNA cluster. [score:8]
Relative expression of miR-17∼92 cluster members and an unrelated microRNA, miR-199, in Adp300- vs AdGFP -expressing cardiac myocytes. [score:5]
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[+] score: 12
For instance, hepatic stellate cells had been found to express miR-199, which influenced stellate cell activity by regulating collagen synthesis and represented a general mechanism contributing to hepatic fibrosis (Lino et al., 2013); the liver sinusoidal endothelial cells also express the miR-199 and this miRNA might serve as a negative regulator of the function of liver sinusoidal endothelial cells in some chemical exposures, such as alcohol (Wang et al., 2012); the increased miR-21 expression was detected in the hepatic stellate cells with the treatment of ethanol and interleukin-6 (Francis et al., 2014). [score:9]
We noticed that ASK1, PKC, and JUN affected by the differentially expressed miRNAs of FMT water extract, i. e., miR-139-5p and miR-199-5p. [score:3]
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[+] score: 11
In order to test whether inhibition of miR199b by LNA‐199b could result in suppression of vascular tube formation in vitro and in vivo, further experiments were performed in the presence of VEGF to induce EC differentiation first following inhibition by LNA‐199b. [score:7]
To elucidate the regulatory role of miR‐199b in EC differentiation, a synthetic precursor for miR‐199b (Pre‐199b) was used to overexpress miR199b. [score:4]
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[+] score: 10
By counting eGFP-anillin expressing CMs, which could be identified according to their H2B-mCh fluorescence, increased cell cycle activity after treatment with miR-199 compared to the scramble miR control could be directly detected without further stainings (Fig.   8b). [score:3]
Further we noticed an increase in the fraction of binucleated CMs in miR-199 -treated CMs (Fig.   8g). [score:1]
Binucleation was determined as 17.7 % of total CMs for miR-199 treatment and only 9.8 % for controls. [score:1]
Ventricles from P2 mice were dissociated and the cells were transfected with either microRNA 199, (miR-199) which was reported to strongly enhance the rate of proliferation in postnatal CMs [10] or scramble miRs as a negative control. [score:1]
Surprisingly, treatment with miR-199 led to an increase of binucleated CMs, indicating induction of cell cycle variations. [score:1]
As a proof of concept, we were able to verify the proliferation-inducing effect of miR-199, as previously published [10]. [score:1]
While in transfections with scramble miRs, a basal cell cycle activity (6.6 %) could be determined, this was significantly (p = 0.0015) enhanced (19.1 %) after transfection with miR-199 (Fig.   8c). [score:1]
b Fluorescence pictures of dissociated αMHC-H2B-mCh/CAG-eGFP-anillin double transgenic hearts (P2), transfected with the cell cycle-modifying miR-199 and a miR-NC. [score:1]
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[+] score: 9
Of the 186 miRNAs the expression of which was altered, nine were up-regulated at both time points (miR-125a-3p, miR-297c, miR-421, miR-452, miR-483, miR-574-3p, miR-574-5p, miR-669a, miR-720) and 11 were down-regulated at both time points (let-7g, miR-107, miR-10a, miR-15a, miR-15b, miR-199b*, miR-26a, miR-29c, miR-324-5p, miR-331-3p, miR-342-3p). [score:9]
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[+] score: 9
On the basis of the opposite functions of CBX7, as oncogene and oncosuppressor, it was not surprising to find that CBX7 was able to regulate in opposite sense miRNAs that have recognized to have oncogenic functions, such as miR-199 (negatively regulated) and miR-155, miR-221 and miR-222 (positively regulated). [score:6]
The results presented in Fig.   1 confirm a drastic overexpression of miR-181, miR-137, miR-199, miR-706 and miR-719 and repression of miR-155 in Cbx7 KO MEFs in comparison with the WT ones. [score:3]
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[+] score: 9
rno-miR-novel-8, rno-homolog-miR-26, and rno-homolog-miR-199 miRNAs were selected from Tier 1, and rno-miR-sno-57 miRNA was selected from Tier 2. In addition, we analysed the expression of miR-741-3p and miR-743a-3p and found that, in accordance with sequencing data, they were highly expressed in rat PSCs. [score:5]
rno-homolog-miR-26 and rno-homolog-miR-199 miRNAs were expressed in EFs, ESCs and iPSCs, which is consistent with the data obtained from sequencing. [score:3]
Four novel miRNAs with the following coordinates: chrX:−:151288045–151288101 (rno-miR-novel-8); chr7:+:70463555–70463594 (rno-homolog-miR-26); chr3:+:16697111–16697143 (rno-homolog-miR-199); and chr18:−:69422790–69422857 (rno-miR-sno-57) were selected for the validation. [score:1]
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[+] score: 8
In recognition that cardiovascular disease and cardiac remo deling is associated with simultaneous dysregulation of several miRNAs (e. g. miR-1, miR-34a, miR-133, miR-199b, miR-320 [11], [15], [36]– [38]) or miRNA families (e. g. miR-34 family [10], miR-208 family [39]), tiny 8-mer seed -targeting LNA-antimiRs could provide an advantage by simultaneous inhibition of entire miRNA seed families [10], [27]. [score:8]
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[+] score: 8
A recent study reported that miR-181a and b, miR-199b, miR-135a and miR-205 targeted endogenous SIRT1 and downregulated its expression in mouse embryonic stem cells [28]. [score:8]
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[+] score: 7
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-29b-1, mmu-mir-30b, mmu-mir-99a, mmu-mir-126a, mmu-mir-132, mmu-mir-141, mmu-mir-181a-2, mmu-mir-185, mmu-mir-193a, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-34c, mmu-let-7d, mmu-mir-196a-1, mmu-mir-196a-2, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-20a, mmu-mir-22, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-34a, mmu-mir-200c, mmu-mir-212, mmu-mir-181a-1, mmu-mir-26a-2, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-378a, mmu-mir-451a, mmu-mir-674, mmu-mir-423, mmu-mir-146b, bta-mir-26a-2, bta-let-7f-2, bta-mir-16b, bta-mir-20a, bta-mir-26b, bta-mir-99a, bta-mir-126, bta-mir-181a-2, bta-mir-199a-1, bta-mir-30b, bta-mir-193a, bta-let-7d, bta-mir-132, bta-mir-199b, bta-mir-200a, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-423, bta-let-7g, bta-mir-200b, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-23b, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-34a, bta-mir-141, bta-mir-146b, bta-mir-16a, bta-mir-185, bta-mir-196a-2, bta-mir-196a-1, bta-mir-199a-2, bta-mir-212, bta-mir-26a-1, bta-mir-29b-1, bta-mir-181a-1, bta-mir-2284i, bta-mir-2284s, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, bta-mir-2284w, bta-mir-2284x, bta-mir-2284y-1, mmu-let-7j, bta-mir-2284y-2, bta-mir-2284y-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2284y-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2284z-4, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285t, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2284ab, bta-mir-2284ac
For example, miR-146b-5p and miR-378a-3p were highly expressed in mouse but they were present at a low level of expression in bovine; inversely, miR-199b-5p, miR-423-5p and miR-193a-5p were weakly expressed in mouse but highly in bovine (Table S2). [score:7]
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[+] score: 7
For example, stcl and Podxl were predicted to be targeted by several inversely regulated miRNAs including mmu-miR-125b-5p, mmu-miR-300-3p, mmu-miR-199a-5p, mmu-miR-199a-5p, mmu-miR-199b-5p, and mmu-miR-214b-5p (Figure 8). [score:4]
Mmu-miR-125b-5p, mmu-miR-34c-5p, mmu-miR-199b-5p, mmu-miR-379-5p, and mmu-miR-127-3p were increased in expression in Sca1 [+]CD31 [−] cells compared to Sca1 [+]CD31 [+] cells. [score:2]
The miRNAs were mmu-miR-125b-5p, mmu-miR-34c-5p, mmu-miR-199b-5p, mmu-miR-379-5p, mmu-miR-127-3p, mmu-miR-322-5p, mmu-miR-20a-5p, mmu-miR-15a-5p, mmu-miR-503-3p, and mmu-miR-204-5p. [score:1]
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[+] score: 7
With these criteria a set of 11 miRNAs (miR-17, miR-33, miR-96, miR-140, miR-181b, miR-183, miR-191, miR-194, miR-199b, miR-341, and miR-1192) were selected that might participate to coordinate with NR2F1 to regulate inner ear gene expression. [score:4]
Of the miRNAs expressed, miR-17 and miR-341 have NR2F1 binding sites within their coding regions, miR-140, miR-191 and miR-199b have NR2F1 binding sites within the proximal promoter region of their loci, and miR-183 and miR-181b have NR2F1 binding sites 8 and 15 base pairs immediately upstream of the transcription start sites, respectively. [score:3]
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[+] score: 7
Alcohol has been shown to downregulate miR-199 in rat liver sinusoidal endothelial cells (LSECs) and human endothelial cells [33]. [score:4]
Decreased miR-199 was associated with increased mRNA expression of endothelin-1 (ET-1) and hypoxia-inducible factor-1 α (HIF-1 α) [33]. [score:3]
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[+] score: 7
Of these, eight (miR-193b, miR-199a-3p/hsa-miR-199b-3p, miR-455-3p, miR-210, miR-381 (also known as miR-381-3p), miR-92a, miR-320c, and miR-136) were upregulated, while the other four (miR-490-5p, miR-4287, miR-BART8*, and miR-US25-1*) were downregulated during this process [22]. [score:7]
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[+] score: 6
Some miRNAs such as miR-122, miR-199 family and MiR-124 is downregulated in HCC and act as putative tumor suppressor genes [15]. [score:6]
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[+] score: 6
Interestingly, the expression of -miR-199b, -miR-199a-5p and –miR-126 in the bovine mammary gland has already been experimentally confirmed. [score:3]
Using the Patrocles database, we found polymorphic miRNA target sites for bta-miR-199b, -miR-199a-5p, and -miR-361 in the IL1B gene and for –miR-126 in the CYP11B1 gene. [score:3]
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[+] score: 6
Hydrogen regulates expressions of miR-9, miR-21, and miR-199, and modifies expressions of IKK-β, NF-κB, and PDCD4 in LPS-activated retinal microglia cells [64]. [score:6]
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[+] score: 6
Comparison of the miRNA expression profiles between the control and SFN treated samples revealed a number of miRNA including miR-214, miR-145, miR-199a, and miR-199b that were significantly upregulated in SFN -treated H460 cells and were reported to be involved in tumorigenesis and progression (Supplementary Figure 3A & 3B). [score:6]
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[+] score: 6
We have shown that in tumor samples compared to normal samples, the majority of miRNAs (miR-216, miR-217, miR-100, miR-345, miR-141, miR-483-3p, miR-26b, miR-150, Let-7b, Let-195 and miR-96) were downregulated, and few were upregulated (miR-146b, miR-205, miR-31, miR-192, miR-194 21, miR-379, miR-431, miR-541, and miR-199b). [score:6]
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[+] score: 6
Recently, several miRNAs including miR-181a and b, miR-9, miR-204, miR-199b, and miR-135a were shown to down-regulate SIRT1 expression in mESC [22]. [score:6]
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[+] score: 6
These transcripts along with miR-199b* were the only miRNAs that were differentially expressed in both comparisons, demonstrating the potential importance of specific subsets of miRNAs in the renewal vs. [score:3]
With the exception of the miR-200 family (i. e. miR-141, -200a, -200b, -200c, -429) and miR-199b*, there was very little overlap in the differentially expressed miRNAs identified from laCL/liCL and ameloblasts/laCL comparisons. [score:3]
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[+] score: 6
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-18a, mmu-mir-199a-2, mmu-mir-18b
Recent association studies between miRNA markers and lung cancer development have demonstrated that the miRNAs miR-18, miR-199, and miR-519c can suppress HIF-1α expression for the purpose of assessing cancer prognosis [39– 41]. [score:6]
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[+] score: 5
Among the miRNAs strongly down-regulated at all tested times were miR-199b-5p (decreased 70-fold), miR-214 (decreased 37-fold), and miR-143 (decreased 13-fold), known to promote differentiation of ESCs, neuroblasts, and smooth muscle progenitors, respectively [46], [47]. [score:4]
Several miRNAs involved in maintenance of pluripotency (miR-294, -146a, -133a) and differentiation (miR-199b-5p, -214, -143) were selected for validation of the microarray results. [score:1]
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[+] score: 5
The array uncovered the induction of 117 miRNAs with the signal intensity ≥500 (the fluorescence amount of each miRNA probe is measured by a photo multiplier tube or charge-coupled device and signal scaled across the range of detection for the platform) in GA muscle (Table 1, Fig. 1A and 1B), including the highly downregulated miRNAs (≥1.5-fold) miR-194-5p, miR-101b-3p, miR-148a-3p, miR-199b-5p, miR-335-5p, miR-127-3p, miR-379-5p, miR-541-5p, miR-382-5p, miR-329-3p, miR-299-5p and miR-434-3p, and the highly up-regulated miRNAs (≥1.5 fold), miR-146b-5p and miR-146a-5p (Fig. 1C). [score:5]
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[+] score: 5
NFATs may also control genes encoding signaling molecules as variate as Ca [2+] regulators [inositol 1,4,5-trisphosphate (IP [3]) receptor (IP [3]R), regulator of calcineurin 1 (RCAN1)], growth factors (VEGF, neurotrophins), myelination genes (P0 and Krox-20), glucose regulation genes (insulin, HNF1, PDX, and GLUT2), cell cycle and death regulator/activators [p21 [Waf1], c-Myc, cyclin -dependent kinase 4 (CDK4), B-cell lymphoma 2 (Bcl-2), and cyclins A2, D1, and D2], oncogenes (Wnt, β-catenin), microRNAs (miR-21, miR-23, miR-24, miR-27, miR-125, miR-195, miR-199, and miR-224), and surfactants (sftpa, sftpb, sftpc, and abca3) [9, 65– 74]. [score:5]
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[+] score: 5
The observed 30% reduction of reporter expression is comparable to the in vitro effects of miR-199b and miR-214, targeting Dyrk1a and Ncx1, respectively, which have been shown to modify cardiac performance (22, 24). [score:5]
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[+] score: 5
It is intriguing to consider the possibility that podocalyxin and DDR1 may be mechanistically linked given that their expression is coordinately suppressed by miR-199b-5p, a microRNA whose loss leads to the elevation of both DDR1 and podocalyxin in acute myeloid leukemia [51]. [score:5]
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[+] score: 5
In this study we have focused on miR-148a, however L5-miRNA targeting could be applied to other miRNAs, such as miR-122, let-7 or miR-199, which have also shown great success in excluding gene expression from the hepatocytes in E1A-miRNA adenoviruses [5, 7, 19- 21]. [score:5]
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[+] score: 5
These include miR-1, miR-133, miR-30 and miR-150 which often show reduced expression, and miR-21, miR-199 and miR-214 which often show increased expression [6], [7], [8], [9], [11], [12], and they may represent miRNAs with a central role in cardiac remo delling. [score:5]
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[+] score: 5
MiR-199b-5p regulates the Hes1 gene, a key effector of the Notch pathway, and inhibits proliferation and survival of MB CD133 [+] cancer-stem-cell populations. [score:3]
We and others have described several miRNAs that are involved in MB development, including miR-125b, miR-324-5p, miR-326 and miR-199b-5p [6], [7], [8]. [score:2]
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[+] score: 5
At 4 months of high-fat diet feeding, 3 miRNAs were upregulated: let7f-5p (FC: 2.3), miR-140-5p (FC: 3.8) and miR-199-3p (FC: 2.1), but two miRNAs were down regulated in obese mice with respect to normal mice: miR-155 (FC: 1.7) and miR-322 (FC: 1.5). [score:5]
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[+] score: 5
Furthermore, up-regulation of miR-199b-5p impaired the development of TICs of medulloblastoma though repression of HES1 [12]. [score:5]
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[+] score: 5
Int J Cancer 29 Chao A Tsai CL Wei PC Hsueh S Chao AS 2009 Decreased expression of microRNA-199b increases protein levels of SET (protein phosphatase 2A inhibitor) in human choriocarcinoma. [score:5]
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[+] score: 4
In addition, down-regulation of miR-199-a-5p and miR-200b upon wounding stimulates repair by increasing cutaneous wound angiogenesis [14, 15]. [score:4]
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[+] score: 4
miR-29 was reported to play a crucial role in CCL4 -induced liver fibrosis 18. miR-199 and 200 family was up-regulated in the progression of liver fibrosis 19. [score:4]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-199a-2
Top 25 predicted targets of miR-199-3p/5p sorted by aggregate P [CT] (DOCX 535 kb) ERK Extracellular signal-regulated kinase. [score:4]
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[+] score: 4
In addition, overexpression of either miRNA-199 or miRNA-590 in the heart of adult mice undergoing MI showed that both miRNAs induced cardiac regeneration and improved cardiac function (36). [score:3]
miRNA-590 and miRNA-199 were further tested and showed to promote cell cycle re-entry of adult cardiomyocytes ex vivo. [score:1]
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[+] score: 4
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-199a-2
Several scientific reports stated the carcinogenic effect of arsenic and its impact on HER-2. For instance, Chuan shu et al., reported that arsenic played a fundamental role to activate signaling mediators including miR-199/148 / ERBB2 / PKM2 / NF-kB to increase the expression of hypoxia-inducible factor 1 (HIF-1), interleukin (IL)-8, and finally increased angiogenesis and contributed to the processes of tumor progression and development (36). [score:4]
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[+] score: 4
This is also in agreement with previous studies showing similar patterns of expression for miR-199 and miR-214 in different systems 15, 20, 21. [score:3]
We searched for conserved putative skeletal transcription factor binding sites (TFBS) in a 2.5 kilobase (kb) region upstream of pre-miR-199 (putative Dnm3os promoter) of human, mouse, Xenopus, medaka, stickleback, Tetraodon, fugu and zebrafish. [score:1]
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[+] score: 4
Lin et al found that miR-199* might affect its target gene Smad1 to regulate chondrogenic differentiation [22]. [score:4]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-214, hsa-mir-200b, mmu-let-7d, mmu-mir-130b, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-141, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, hsa-mir-200c, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-200a, hsa-mir-130b, hsa-mir-376a-1, mmu-mir-376a, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, hsa-mir-429, mmu-mir-429, hsa-mir-450a-1, mmu-mir-450a-1, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-130b, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, hsa-mir-450a-2, dre-let-7j, hsa-mir-376a-2, mmu-mir-450a-2, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
The most abundant miRs expressed in the developing mouse OE are: the miR-200-class (- 200a, - 200b, - 200c, - 141 and - 429), miR-199, miR-152, miR-214, miR-205, miR-183, miR-182 and miR-96 (Choi et al., 2008). [score:3]
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[+] score: 3
Only a few miRNA from the selected group had validated target genes: miR-155, miR-21, miR-125a, miR-31, miR-205, miR-20a, let-7f, miR-182, let-7e, miR-199b, miR-199a, miR-663, and miR-193a. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-148b, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The 3′ UTR of mouse Xbp1 mRNA contains several putative target sites for miR-199, miR-299, miR-433, miR-221, and miR-490. [score:3]
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[+] score: 3
For instance, miR-125b-5p, miR-199b, and miR-378-3p showed elevated expression in nematode infection-elicited alternative macrophage activation [19]. [score:3]
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[+] score: 3
In the current study Let-7b was increased and two additional putative OPRM1 mRNA targeting miRNAs were decreased [miR-154 and miR-199b, (He and Wang, 2012)] but not miR-134, (Ni et al., 2013). [score:3]
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[+] score: 3
For example, miRNA-21, miRNA-23a, miRNA-24, miRNA-133, miRNA-208/miRNA-195 and miRNA-199 have been shown to be involved in cardiac hypertrophy (15- 17), miRNA-1 in arrhythmia (18), miRNA-29 and miRNA-21 in cardiac fibrosis (19, 20), miRNA-210 and miRNA-494 in ischemic heart disease (21) and miRNA-129 in heart failure (22). [score:3]
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[+] score: 3
As shown in Additional file 4: Table S4, the trend of expression of mir-21, mir-200, mir-199, and mir-31 is confirmed. [score:3]
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[+] score: 3
ZNF91 belongs to a C [2]H [2] zinc finger (ZNF) gene family that is greatly expanded in the primate lineage and known to contain exceptionally abundant target sites for several miRNA families, including miR-23, miR-181 and miR-199 [28]. [score:3]
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[+] score: 3
The progression of liver fibrosis is related with overexpression of the miR-199 and 200 families. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Other miRNAs from this paper: mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-141, mmu-mir-152, mmu-mir-182, mmu-mir-183, mmu-mir-191, mmu-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-let-7d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-96, mmu-mir-200c, mmu-mir-214, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, dre-mir-7b, dre-mir-7a-1, dre-mir-7a-2, dre-mir-182, dre-mir-183, dre-mir-199-1, dre-mir-199-2, dre-mir-199-3, dre-mir-205, dre-mir-214, dre-mir-430a-1, dre-mir-430b-1, dre-mir-430c-1, mmu-mir-429, mmu-mir-449a, dre-mir-429a, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-7a-3, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-141, dre-mir-152, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-430c-2, dre-mir-430c-3, dre-mir-430c-4, dre-mir-430c-5, dre-mir-430c-6, dre-mir-430c-7, dre-mir-430c-8, dre-mir-430c-9, dre-mir-430c-10, dre-mir-430c-11, dre-mir-430c-12, dre-mir-430c-13, dre-mir-430c-14, dre-mir-430c-15, dre-mir-430c-16, dre-mir-430c-17, dre-mir-430c-18, dre-mir-430a-2, dre-mir-430a-3, dre-mir-430a-4, dre-mir-430a-5, dre-mir-430a-6, dre-mir-430a-7, dre-mir-430a-8, dre-mir-430a-9, dre-mir-430a-10, dre-mir-430a-11, dre-mir-430a-12, dre-mir-430a-13, dre-mir-430a-14, dre-mir-430a-15, dre-mir-430a-16, dre-mir-430a-17, dre-mir-430a-18, dre-mir-430i-1, dre-mir-430i-2, dre-mir-430i-3, dre-mir-430b-2, dre-mir-430b-3, dre-mir-430b-4, dre-mir-430b-6, dre-mir-430b-7, dre-mir-430b-8, dre-mir-430b-9, dre-mir-430b-10, dre-mir-430b-11, dre-mir-430b-12, dre-mir-430b-13, dre-mir-430b-14, dre-mir-430b-15, dre-mir-430b-16, dre-mir-430b-17, dre-mir-430b-18, dre-mir-430b-5, dre-mir-430b-19, dre-mir-430b-20, dre-let-7j, mmu-mir-449c, mmu-mir-449b, dre-mir-429b, mmu-let-7j, mmu-let-7k, mmu-mir-124b
By contrast, we identified 12 miRNAs corresponding to 9 families (miR-199, miR-140, miR-152, miR-214, miR-205, miR-200, miR-183, miR-182, miR-96) that displayed highly enriched expression in the olfactory system (Figure 1A). [score:3]
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[+] score: 3
Mir-199b shows upregulation in p53R172H iPS. [score:3]
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[+] score: 2
The expression profile of 3 out of 13 commonly modulated miRNAs, miR-199-3p, miR-214, and miR-376a that have been shown to be important in brain related processes and functions was also validated using the singleplex miRNA assay (Life Technologies, Carlsbad, CA) (Figure 7). [score:2]
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[+] score: 2
Microarray data were validated by real time-qPCR for miR- 146a, miR-191, miR-199b, and miR-223 as previously described [27]. [score:1]
The results of qPCR analyses carried out by testing the RNA samples of mice from 6 experimental groups (Sham, Aspirin, Naproxen, ECS, ECS + Aspirin, and ECS + Naproxen) for miR- 146a, miR-191, miR-199b, and miR-223 are shown in Figure 5. Although the differences among groups were more attenuated, qPCR analyses confirmed the microarray data. [score:1]
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[+] score: 2
Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, mmu-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
For instance, the human genome has 3 paralogous mir-199 genes. [score:1]
hsa-mir-199a-2 has defined orthologs in both mouse and rat, and hsa-mir-199b is orthologous to mmu-mir-199b. [score:1]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-199a-1, mmu-mir-199a-2
Baumgarten A. Bang C. Tschirner A. Engelmann A. Adams V. von Haehling S. Doehner W. Pregla R. Anker M. S. Blecharz K. TWIST1 regulates the activity of ubiquitin proteasome system via the miR-199/214 cluster in human end-stage dilated cardiomyopathyInt. [score:2]
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[+] score: 2
By using quantitative real-time RT-PCR analysis, we found that a collection of miRNAs were regulated by IPost (Figure 1), such as miR-21, miR-15b, and miR-199b. [score:2]
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[+] score: 1
From the following groups of miRNAs with identical sequence, only the first member is annotated in the heat-map: mmu-let-7a*/mmu-let-7c-2*; mmu-miR-466a-3p/mmu-miR-466b-3p/mmu-miR-466c-3p/mmu-miR-466e-3p; mmu-miR-467a*/mmu-miR-467d*; mmu-miR-297a*/mmu-miR-297c*/mmu-miR-297b-3p and mmu-miR-199a-3p/mmu-miR-199b. [score:1]
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[+] score: 1
Dnm3os ncRNA host gene for microRNAs, miR-199 and miR-214. [score:1]
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[+] score: 1
Interestingly, we found among them several previously OA -associated miRs such as miR-27b, miR-199, miR-29a, miR-26, and miR-365 [16, 17]. [score:1]
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[+] score: 1
Other miRNAs from this paper: mmu-mir-141, mmu-mir-34c, mmu-mir-34b, mmu-mir-34a
Previously, only the roles of miR-141 and miR-199b in choriocarcinoma were reported [7, 8]. [score:1]
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[+] score: 1
Nevertheless, the MSCs+si-H19 group showed a significantly elevated level of miR-199-5p in contrast to the MSCs+si-H19 NC and MSCs groups (P < 0.01, Fig.   7c). [score:1]
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[+] score: 1
MiR-125a-5p is transcribed as a cluster with let-7 and miR-199b. [score:1]
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[+] score: 1
Additionally, miR-23a [15], miR-24 [16], miR-26 [17], miR-27a [18, 19], miR-27b [20], miR-29 [21], miR-124 [22], miR-128a [23], miR-146b [24], miR-148a [25], miR-155 [26], miR-181 [27], miR-199 [28], miR-186 [29], miR-214 [30], miR-221/222 [31], miR-351 [32], miR-486 [33], miR-489 [34], miR-499 [35] and miR-3906 [36] are reported to be involved in skeletal myogenesis. [score:1]
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[+] score: 1
Other miRNAs from this paper: mmu-mir-21a, mmu-mir-21b, mmu-mir-21c
Candidate miRNAs that could mediate Notch-activating signaling may include miRNA199b-5p [62] or miRNA-21 [63]. [score:1]
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[+] score: 1
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-27a, hsa-mir-29a, hsa-mir-101-1, dme-mir-1, dme-mir-2a-1, dme-mir-2a-2, dme-mir-2b-1, dme-mir-2b-2, dme-mir-10, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-101a, mmu-mir-124-3, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-137, mmu-mir-140, mmu-mir-142a, mmu-mir-155, mmu-mir-10b, mmu-mir-183, mmu-mir-193a, mmu-mir-203, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-183, hsa-mir-199b, hsa-mir-203a, hsa-mir-210, hsa-mir-222, hsa-mir-223, dme-mir-133, dme-mir-34, dme-mir-124, dme-mir-79, dme-mir-210, dme-mir-87, mmu-mir-295, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, dme-let-7, dme-mir-307a, dme-mir-2c, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-126, hsa-mir-193a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-29a, mmu-mir-27a, mmu-mir-34a, mmu-mir-101b, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-155, mmu-mir-10a, mmu-mir-210, mmu-mir-223, mmu-mir-222, mmu-mir-124-1, mmu-mir-124-2, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-378a, mmu-mir-378a, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-411, hsa-mir-193b, hsa-mir-411, mmu-mir-193b, hsa-mir-944, dme-mir-193, dme-mir-137, dme-mir-994, mmu-mir-1b, mmu-mir-101c, hsa-mir-203b, mmu-mir-133c, mmu-let-7j, mmu-let-7k, mmu-mir-126b, mmu-mir-142b, mmu-mir-124b
of 5′-isomiR reads Arm abundance hsa-miR-203 GAAAUGU 3p 8 8,774,451 45.5 hsa-miR-140 CCACAGG 3p 37 1,072,944 39.5 hsa-miR-126 GUACCGU 3p 54 776,502 13.8 hsa-miR-199b ACAGUAG 3p 55 724,009 27.0 hsa-miR-101 UACAGUA 3p 57 662,855 27.3 hsa-miR-10a CCCUGUA 5p 59 661,921 22.7 hsa-miR-143 UGAGAUG 3p 69 619,911 1.8 hsa-miR-378a UGGACUU 3p 71 402,197 6.0 hsa-miR-29a UAGCACC 3p 77 334,605 18.1 hsa-let-7a AGGUAGU 5p 89 269,329 0.6 The arm abundance of a 5′-isomiR is the percentage of all reads mapped to one arm that represents the 5′-isomiR. [score:1]
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